March 22 - Cardiology

Question 1

Endothelium-mediated vasodilation

Answer 1

1. ACh, bradykinin, serotonin, substance P, shear forces increase Ca++ leading to eNOS activation
2. eNOS synthesizes NO from argininine, NADPH, and O2
3. NO activates guanalyl cyclase, increasing cGMP and decreasing Ca++ in VSMC and decreasing contraction

Question 2

ARB MOA

Answer 2

blocks ang II receptors. Ang II levels increase but its effects are blocked

Question 3

Aortic regurn

Answer 3

Early diastolic murmur. Duration of murmur indicative of severity. Most common cause is aortic root dilation

Question 4

Small vs large VSD

Answer 4

Small

• holosystolic murmur at L sternal border
• insignificant, close spontaneously

Large

• no murmur
• failure to thrive, diaphoresis with feeding

Question 5

Why CCBs don’t affect skeletal muscle

Answer 5

Skeletal muscle not dependent on extracellular Ca++. It is the interaction between L-type Ca++ channels in the plasma membrane and RyR channels in the SR that matters

Question 6

Pathologic progression post-MI

Answer 6

First 4 hours: normal myocardium
4-12 hours: cytoplasmic hypereosinophilia, edema, punctate hemorrhage (early coag necrosis)
12-24 hours: continued coag necrosis, marginal contraction band necrosis
1-5 days: coag necrosis + neutrophil infiltrate
5-10 days: macrophages
10-14 days: granulation tissue and neovascularization
2 wks to 2 mos: scar formation

Question 7

Doxorubicin cardiotoxicity

Answer 7

Causes dilated cardiomyopathy. Prevented with dexrazoxane (iron chelator that decreases free radical formation)

Question 8

Nitrate dosing

Answer 8

Round the clock nitrates results in rapid development of tolerance. Thus, when nitrates used chronically, provide a daily nitrate-free interval typically overnight

Question 9

Use dependence of different class I antiarrythmics

Answer 9

Highest with class IC due to slow dissociation/strongest binding strength to Na+ channels. IB dissociate the most rapidly due to weakest binding strength

Question 10

Causes of S3 heart sound

Answer 10

1. Forceful or rapid filling
2. Decreased ventricular compliance
   3) Increased ESV

Question 11

Pulmonary HTN due to LHF: pathogenesis

Answer 11

Pulmonary venous congestion increases pulmonary capillary and arterial pressure. High pressures damage the endothelium, increasing vascular tone and causing remodeling with smooth muscle proliferation

Question 12

Janeway lesions

Answer 12

Nontender macules on the palms and soles caused by septic emboli from valvular vegetations

Question 13

Signs of acute vs chronic pericarditis

Answer 13

Acute: pleuritic chest pain, pericardial friction rub

Chronic (months to years): paradoxic increase in JVP with inspiration, pulsus paradoxus, pericardial knock

Question 14

pulsus paradoxus

Answer 14

Decrease in systolic BP greater thn 10 during inspiration. Associated with cor pulmonale, chronic constrictive pericarditis, cardiac tamponade

Question 15

Atherosclerosis pathogenesis

Answer 15

1. Endothelial cell injury. Can be caused by HTN, hyperlipidemia, smoking, diabetes, others
2. Increased vascular permeability allows for leukocyte adhesion and migration. Exposure of subendothelial collagen allows for platelet adhesion.
3. Medial smooth muscle migrates to the intima. LDL also migrates to intima and is endocytosed by macrophages yielding foam cells.
4. Chronic inflammatory state is maintained by macrophage and lymphocyte release of cytokines and growth factors. These cause continued deposition of LDL, SMC proliferation and production of more ECM, and foam cell necrosis and release of lipids into the intima ECM

Question 16

Varicose veins: pathogenesis, risk factors, complications

Answer 16

Pathogenesis: Increased pressure results in venous dilation causing stretching and failure of the venous valves. Results in venous stasis, congestion, and lower extremity edema.

Risk factors: Long periods of standing, age over 50, obesity, multiple pregnancies (all things that increase venous pressure in legs chronically)

Complications: Thromboses, stasis dermatitis, skin ulcers, poor wound healing, superficial infection. No risk of DVT or PE because varicosities are in superficial, not deep veins

Question 17

Pericardial disease: etiology

Answer 17

Infection
Autoimmune - RA, SLE, Dressler syndrome post-MI
Direct trauma
Cancer - lung, breast, esophageal, lymphoma

Question 18

Acute pericarditits

Answer 18

Inflammatin of pericardium. Presents with friction rub and pleuritic, positional chest pain. Detected on EKG with global ST elevation and PR depression. Treated wtih anti-inflammatories (NSAIDs first, glucocorticoids if ineffective)

Question 19

Pericardial effusion

Answer 19

Fluid between pericardium and myocardium. Ranges from mild to cardiac tamponade at severe end. Can be due to underlying pericarditis or to traumatic injury or ventricular free wall rupture after MI. Hemodynamic problem: pressure prevents ventricular filling. Treatment is fliuds which can help with ventricular filling, treating underlying etiology, and/or pericardiocentesis/surgery

Question 20

Chronic pericarditis

Answer 20

Result of chronic pericardial inflammation that leads to fibrosis of pericardium. Can prevent diastolic filling. Pericardial knock results from relaxation of ventricle against fibrotic pericardium. Anatomic problem with anatomic solution (removal of pericardium)

Question 21

MOA of ANP and BNP

Answer 21

Activate guanylate cyclase, increasing cGMP, leading to vasodilation. Also cause diuresis.

Question 22

Myocardial hybernation

Answer 22

State of chronic myocardial ischmiea Myocardial metabolism and function decrease to match the decrease seen in coronary bood flow. Prevents myocardial necrosis

Question 23

Isolated atrial amyloidosis

Answer 23

Deposition of abnormally folded ANP. Incidence increases with age. Can increase risk of afib

Question 24

Statin MOA

Answer 24

Inhibits hepatic cholesterol synthesis. LDL receptor expression increases in liver leading to increased LDL uptake and lower serum cholesterol and LDL

Question 25

Osler-Weber-Rendu syndrome

Answer 25

another name for HHT

Question 26

Von recklinghausen’s disease

Answer 26

another name for NF1

Question 27

EKG patterns for different MIs

Answer 27

PDA occlusion: causes inferior wall ischemia which manifests as ST elevation in II, III, and aVF

LAD occliusion: causes anterior wall ischemia which manifests as ST elevation in V1-V4

LCX occlusion: causes lateral wall ischemia which manifests as ST elevation in V5-V6, sometimes I and aVL

Question 28

LPL

Answer 28

Enzyme that hydrolyzes TGs, releasing FFAs and facilitates cholesterol transfer to HDL

Question 29

Cardiac myxoma

Answer 29

Most commonly arises in LA as a large, gelatinous, pedunculated mass. Histology shows scattered cells in mucopolysaccharide stroma, abnormal BVs, and hemorrhage. Presents with constitutional symptoms, murmur, and positional dyspnea due to valve obstruction

Question 30

Kussmaul sign

Answer 30

Volume constricted RV in chronic pericarditis can’t accomodate increased venous return during inspiration, resulting in JVD